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作 者:刁尧[1] 刘新宇[1] 赵文瑾[1] 刘杰[1] 赵恂[1] 于成国[1]
机构地区:[1]中国医科大学实验技术中心,辽宁沈阳110001
出 处:《中国现代医学杂志》2011年第29期3615-3617,3626,共4页China Journal of Modern Medicine
基 金:辽宁省自然科学基金资助项目(No:20092118)
摘 要:目的观察超氧化物歧化酶类似物锰四(4-苯甲酸)卟啉(MnTBAP)对脑挫伤大鼠脑组织中丙二醛(MDA)、超氧化物歧化酶(SOD)及一氧化氮(NO)含量的影响,探讨MnTBAP对脑挫伤后继发性损伤的保护作用。方法 SD大鼠60只,雌雄不拘,分为假手术对照组、损伤组和MnTBAP治疗组。用自由落体方法制备大鼠脑挫伤模型,损伤组术后立即腹腔注射生理盐水,治疗组术后立即腹腔注射MnTBAP(10 mg/kg体质量)。于术后1、6、12和24 h取挫伤侧脑组织标本,测定SOD、MDA和NO活性和含量。结果与假手术对照组相比,损伤组脑组织SOD水平降低(P<0.01),MDA和NO水平增高(P<0.01)。与损伤组相比,MnTBAP治疗组脑组织SOD水平增高(P<0.05),相反,MDA和NO水平降低(P<0.01)。结论 MnTBAP具有抗氧化清除自由基功能,能有效提高挫伤后脑组织SOD含量,减少MDA和NO含量,对继发性脑损伤具有保护作用。[Objective] To observe the effects of MnTBAP on MDA, SOD and NO level of brain tissues in rats with cerebral trauma. [Methods] Sixty rats were divided into three groups: sham-operated group, cerebral trauma group, and MnTBAP treat group. All cerebral traumatic models were in free fall injury way. Then the normal saline, MnTBAP (10 mg/kg) were given intraperitoneally immediately in cerebral traumatic group, treated group respectively. At 1, 6, 12, 24 hours following cerebral trauma, five rats in each group were sac- rificed and the injured segments were resected for measuring SOD, MDA and SOD. [Results] Activity of SOD was reduced significantly (P〈0.01), and the level of MDA and NO were increased significantly (P〈0.01) in the injured cerebral tissue following cerebral trauma. MnTBAP were obviously prevent reduction of SOD activity (P〈0.05), reduce the production of MDA (P〈0.01), and inhabit the NO level (P〈0.01) in comparison with the cerebral trauma model. [Conclusion] MnTBAP may effectively prevent reduction of SOD actively, reduce the production of MDA, and inhabit the NO level in brain tissues after trauma, so as to exert its therapeutic effects.
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